Congestive Heart Failure (CHF) refers to a clinical syndrome of symptomatic events associated with compromised cardiac function. The term “heart failure” may describe the inability of the heart to supply sufficient blood flow to meet the physiological needs of the peripheral tissues. Heart failure may be associated with either systolic dysfunction or diastolic dysfunction. In some cases, both systolic and diastolic dysfunction may coexist.
Systolic dysfunction refers to the inability of the cardiac contractile mechanism to develop adequate force, e.g., the inability to overcome mechanical afterload. The heart may compensate for reduced systolic dysfunction by dilating or stretching in order to improve ejection by increasing preload via the Frank-Starling mechanism. Thus, systolic dysfunction may often be characterized by a dilated, thin-walled ventricle with low ejection fraction.
Diastolic dysfunction refers to the inability of a ventricle to adequately fill. Diastolic dysfunction may arise from several mechanisms, including hypertension. Increased afterload due to increased systemic vascular resistance or reduced arterial compliance can lead to increased wall stress according to the Law of LaPlace. The ventricle may compensate for such increased wall stress by thickening or hypertrophying. Thus, diastolic ventricular dysfunction may often be characterized by ventricular hypertrophy and perhaps increased ejection fraction.
The myocardium may be thought of as a viscoelastic material with time-varying mechanical properties that rhythmically contracts against an incompressible fluid (blood), itself contained in viscoelastic network of blood vessels. Ventricular “preload” describes the stretch on the myocardial fibers just prior to contraction. Preload may be estimated clinically as left ventricular end diastolic volume (LVEDV).
Both systolic and diastolic dysfunction can lead to symptoms of CHF. Both may also be associated with increased ventricular filling pressures and volumes. However, systolic dysfunction may be closely associated with left ventricle (LV) dilation (i.e., increased preload), while diastolic dysfunction may be associated with reduced LV end diastolic volume.
Proposed techniques to estimate cardiac chamber or vascular pressure rely on invasive placement of high fidelity micronanometer transducers directly into the chamber of interest including the ventricles, atria or great vessels. It has been proposed to incorporate such transducers onto standard implantable pacemaker or pacemaker-cardioverter-defibrillator leads or lead configurations. This may increase the size of the lead, or may require the placement of one or more additional leads (compared to a standard device implant) for pressure monitoring. Measurements of cardiac chamber dimension typically require acute invasive or non-invasive test equipment such as ventriculography, echocardiography, or magnetic resonance imaging.